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| In all eukaryotic cells, intracellular Ca2+ levels are maintained at low resting concentrations (approximately 100 nM) by the activity of the major Ca2+ extrusion system, the plasma membrane Ca2+-ATPase (PMCA), which exchanges extracellular protons (H+) for cytosolic Ca2+. Indeed, sustained elevation of [Ca2+]C in the form of overload, saturating all Ca2+-dependent effectors, prolonged decrease in [Ca2+]ER, causing ER stress response, and high [Ca2+]M, inducing mitochondrial permeability transition (MPT), are considered to be pro-death factors. In cancer the Ca2+-handling toolkit undergoes profound remodelling (figure 1) to favour activation of Ca2+-dependent transcription factors, such as the nuclear factor of activated T cells (NFAT), c-Myc, c-Jun, c-Fos that promote hypertrophic growth via induction of the expression of the G1 and G1/S phase transition cyclins (D and E) and associated cyclin-dependent kinases (CDK4 and CDK2). Thus, cancer cells may evade apoptosis through decreasing calcium influx into the cytoplasm. This can be achieved by either downregulation of the expression of plasma membrane Ca2+-permeable ion channels or by reducing the effectiveness of the signalling pathways that activate these channels. Such protective measures would largely diminish the possibility of Ca2+ overload in response to pro-apoptotic stimuli, thereby impairing the effectiveness of mitochondrial and cytoplasmic apoptotic pathways. Voltage-Gated Calcium Channels (VGCCs): Overexpression of VGCCs has been associated with increased tumor growth and metastasis in various cancers, including breast and prostate cancer. Store-Operated Calcium Entry (SOCE): SOCE mechanisms, such as STIM1 and ORAI1, are often upregulated in cancer cells, contributing to enhanced cell survival and proliferation. High intracellular calcium levels are associated with increased cell proliferation and migration, leading to a poorer prognosis. Calcium signaling can also influence hormone receptor status, affecting treatment responses. Increased Ca²⁺ signaling is associated with advanced disease and metastasis. Patients with higher CaSR expression may have a worse prognosis due to enhanced tumor growth and resistance to apoptosis. -Ca2+ is an important regulator of the electric charge distribution of bio-membranes. |
| 5270- | 5-ALA, | PDT, | 5-Aminolevulinic Acid as a Theranostic Agent for Tumor Fluorescence Imaging and Photodynamic Therapy |
| - | Review, | Var, | NA |
| 3864- | ACNs, | Anthocyanins Potentially Contribute to Defense against Alzheimer’s Disease |
| - | Review, | AD, | NA |
| 319- | AgNPs, | Endoplasmic reticulum stress signaling is involved in silver nanoparticles-induced apoptosis |
| 346- | AgNPs, | RSQ, | Investigating Silver Nanoparticles and Resiquimod as a Local Melanoma Treatment |
| - | in-vivo, | Melanoma, | SK-MEL-28 | - | in-vivo, | Melanoma, | WM35 |
| - | in-vitro, | neuroblastoma, | SH-SY5Y |
| 400- | AgNPs, | MF, | Polyvinyl Alcohol Capped Silver Nanostructures for Fortified Apoptotic Potential Against Human Laryngeal Carcinoma Cells Hep-2 Using Extremely-Low Frequency Electromagnetic Field |
| - | in-vitro, | Laryn, | HEp2 |
| 2288- | AgNPs, | Silver Nanoparticle-Mediated Cellular Responses in Various Cell Lines: An in Vitro Model |
| - | Review, | Var, | NA |
| 5356- | AL, | Therapeutic role of allicin in gastrointestinal cancers: mechanisms and safety aspects |
| - | Review, | GC, | NA |
| 2655- | AL, | Allicin and Digestive System Cancers: From Chemical Structure to Its Therapeutic Opportunities |
| - | Review, | GC, | NA |
| 2656- | AL, | Allicin Protects PC12 Cells Against 6-OHDA-Induced Oxidative Stress and Mitochondrial Dysfunction via Regulating Mitochondrial Dynamics |
| - | in-vitro, | Park, | PC12 |
| 2658- | AL, | The Toxic Effect Ways of Allicin on Different Cell Lines |
| - | Review, | Var, | NA |
| 3271- | ALA, | Decrypting the potential role of α-lipoic acid in Alzheimer's disease |
| - | Review, | AD, | NA |
| 2631- | Api, | Apigenin Induces Autophagy and Cell Death by Targeting EZH2 under Hypoxia Conditions in Gastric Cancer Cells |
| - | in-vivo, | GC, | NA | - | in-vitro, | GC, | AGS |
| 2632- | Api, | Apigenin inhibits migration and induces apoptosis of human endometrial carcinoma Ishikawa cells via PI3K-AKT-GSK-3β pathway and endoplasmic reticulum stress |
| - | in-vitro, | EC, | NA |
| 2633- | Api, | Apigenin induces ROS-dependent apoptosis and ER stress in human endometriosis cells |
| - | in-vitro, | EC, | NA |
| 2634- | Api, | Apigenin induces both intrinsic and extrinsic pathways of apoptosis in human colon carcinoma HCT-116 cells |
| - | in-vitro, | CRC, | HCT116 |
| 2639- | Api, | Plant flavone apigenin: An emerging anticancer agent |
| - | Review, | Var, | NA |
| 2640- | Api, | Apigenin: A Promising Molecule for Cancer Prevention |
| - | Review, | Var, | NA |
| 3887- | Api, | The flavonoid apigenin protects brain neurovascular coupling against amyloid-β₂₅₋₃₅-induced toxicity in mice |
| - | in-vivo, | AD, | NA |
| 3383- | ART/DHA, | Dihydroartemisinin: A Potential Natural Anticancer Drug |
| - | Review, | Var, | NA |
| 5381- | ART/DHA, | Artemisitene triggers calcium-dependent ferroptosis by disrupting the LSH-EWSR1 interaction in colorectal cancer |
| - | in-vitro, | CRC, | HCT116 | - | in-vitro, | Nor, | NCM460 | - | in-vitro, | CRC, | HT29 | - | in-vitro, | CRC, | HCT8 |
| 5362- | AV, | Anti-cancer effects of aloe-emodin: a systematic review |
| - | Review, | Var, | NA |
| 1098- | BA, | Baicalein inhibits fibronectin-induced epithelial–mesenchymal transition by decreasing activation and upregulation of calpain-2 |
| - | in-vitro, | Nor, | MCF10 | - | in-vivo, | NA, | NA |
| 5502- | Ba, | An overview of pharmacological activities of baicalin and its aglycone baicalein: New insights into molecular mechanisms and signaling pathways |
| - | Review, | Var, | NA |
| 1532- | Ba, | Baicalein as Promising Anticancer Agent: A Comprehensive Analysis on Molecular Mechanisms and Therapeutic Perspectives |
| - | Review, | NA, | NA |
| 2478- | Ba, | The role of Ca2+ in baicalein-induced apoptosis in human breast MDA-MB-231 cancer cells through mitochondria- and caspase-3-dependent pathway |
| - | in-vitro, | BC, | MDA-MB-231 |
| 2474- | Ba, | Anticancer properties of baicalein: a review |
| - | Review, | Var, | NA | - | in-vitro, | Nor, | BV2 |
| 2606- | Ba, | Baicalein: A review of its anti-cancer effects and mechanisms in Hepatocellular Carcinoma |
| - | Review, | HCC, | NA |
| 2601- | Ba, | Cardioprotective effects of baicalein on heart failure via modulation of Ca2 + handling proteins in vivo and in vitro |
| - | in-vitro, | Nor, | NA | - | in-vivo, | Nor, | NA |
| 2600- | Ba, | Baicalein Induces Apoptosis and Autophagy via Endoplasmic Reticulum Stress in Hepatocellular Carcinoma Cells |
| - | in-vitro, | HCC, | SMMC-7721 cell | - | in-vitro, | HCC, | Bel-7402 |
| 2617- | Ba, | Potential of baicalein in the prevention and treatment of cancer: A scientometric analyses based review |
| - | Review, | Var, | NA |
| 2296- | Ba, | The most recent progress of baicalein in its anti-neoplastic effects and mechanisms |
| - | Review, | Var, | NA |
| 5544- | BBM, | Berbamine promotes macrophage autophagy to clear Mycobacterium tuberculosis by regulating the ROS/Ca2+ axis |
| - | in-vitro, | AML, | THP1 |
| 1379- | BBR, | Berberine derivative DCZ0358 induce oxidative damage by ROS-mediated JNK signaling in DLBCL cells |
| - | in-vitro, | lymphoma, | NA |
| 1402- | BBR, | Berberine-induced apoptosis in human glioblastoma T98G cells is mediated by endoplasmic reticulum stress accompanying reactive oxygen species and mitochondrial dysfunction |
| - | in-vitro, | GBM, | T98G |
| 2689- | BBR, | Berberine protects against glutamate-induced oxidative stress and apoptosis in PC12 and N2a cells |
| - | in-vitro, | Nor, | PC12 | - | in-vitro, | AD, | NA | - | in-vitro, | Stroke, | NA |
| 2670- | BBR, | Berberine: A Review of its Pharmacokinetics Properties and Therapeutic Potentials in Diverse Vascular Diseases |
| - | Review, | Var, | NA |
| 2684- | BBR, | Berberine is a Novel Mitochondrial Calcium Uniporter Inhibitor that Disrupts MCU‐EMRE Assembly |
| - | in-vivo, | Nor, | NA |
| 5177- | BBR, | Berberine induces apoptosis in human HSC-3 oral cancer cells via simultaneous activation of the death receptor-mediated and mitochondrial pathway |
| - | in-vitro, | Oral, | HMC3 |
| 2720- | BetA, | Betulinic acid induces apoptosis of HeLa cells via ROS-dependent ER stress and autophagy in vitro and in vivo |
| - | in-vitro, | Cerv, | HeLa |
| 2732- | BetA, | Chemo, | Betulinic acid chemosensitizes breast cancer by triggering ER stress-mediated apoptosis by directly targeting GRP78 |
| - | in-vitro, | BC, | MCF-7 | - | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | Nor, | MCF10 |
| 2735- | BetA, | Betulinic acid as apoptosis activator: Molecular mechanisms, mathematical modeling and chemical modifications |
| - | Review, | Var, | NA |
| 5476- | BM, | In Vitro Synergistic Inhibition of HT-29 Proliferation and 2H-11 and HUVEC Tubulogenesis by Bacopaside I and II Is Associated with Ca2+ Flux and Loss of Plasma Membrane Integrity |
| - | vitro+vivo, | CRC, | HT29 |
| 3509- | Bor, | Boron and Prostate Cancer a Model for Understanding Boron Biology |
| - | NA, | Pca, | NA |
| 3511- | Bor, | Boron |
| - | Review, | NA, | NA |
| 3512- | Bor, | Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake |
| - | in-vitro, | Pca, | DU145 |
| 3521- | Bor, | A new hope for obesity management: Boron inhibits adipogenesis in progenitor cells through the Wnt/β-catenin pathway |
| - | in-vitro, | Obesity, | 3T3 |
| 696- | Bor, | Nothing Boring About Boron |
| - | Review, | Var, | NA |
| 746- | Bor, | Organoboronic acids/esters as effective drug and prodrug candidates in cancer treatments: challenge and hope |
| - | Review, | NA, | NA |
| 760- | Bor, | Therapeutic Efficacy of Boric Acid Treatment on Brain Tissue and Cognitive Functions in Rats with Experimental Alzheimer’s Disease |
| - | in-vivo, | AD, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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